Research Paper Volume 11, Issue 24 pp 11865—11879
MicroRNA 27b promotes cardiac fibrosis by targeting the FBW7/Snail pathway
- 1 Department of Cardiovascular Surgery, The General Hospital of Tianjin Medical University, Tianjin, China
- 2 Department of Anatomy and Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China
- 3 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China
- 4 College of Life and Health Sciences, Anhui Science and Technology University, Chuzhou, Anhui, China
- 5 Department of Cardiology, The 2nd Medical Centre, PLA General Hospital, Beijing, China
Received: July 19, 2019 Accepted: November 8, 2019 Published: December 23, 2019https://doi.org/10.18632/aging.102465
How to Cite
Copyright © 2019 Fu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Our study aspires to understand the impact of miR-27b on myocardial fibrosis as well as its functional mechanism. 12 days post the ligation of coronary artery in rats, the expression of miR-27b in the peri-infarction region was elevated. Treating cultivated rat neonatal cardiac fibroblasts (CFs) with angiotensin II (AngII) also enhanced the miR-27b expression. Forced expression of miR-27b promoted the proliferation and collagen production in rat neonatal CFs, as revealed by cell counting, MTT assay, and quantitative reverse transcription-polymerase chain reaction. FBW7 was found to be the miR-27b’s target since the overexpression of miR-27b reduced the transcriptional level of FBW7. The enhanced expression of FBW7 protein abrogated the effects of miR-27b in cultured CFs, while the siRNA silence of FBW7 promoted the pro-fibrosis activity of AngII. As to the mechanism, we found that the expression of FBW7 led to the degradation of Snail, which is an important regulator of cardiac epithelial-mesenchymal transitions. Importantly, inhibition of miR-27b abrogated the coronary artery ligation (CAL) induced cardiac fibrosis in vivo, suggesting that it might be a potential target for the treatment of fibrosis associated cardiac diseases.